Extensive genetic alterations in prostate cancer revealed by dual PCR and FISH analysis

Macoska, Jill A.; Micale, Mark A.; Sakr, Wael; Benson, Philip; Wolman, Sandra R.

doi:10.1002/gcc.2870080205

Cited by 68 publications

(39 citation statements)

References 18 publications

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“…Cytogenetic and molecular genetic studies have demonstrated that gains of chromosome 7 and 7 q-arm alterations were frequent in prostate cancer (30,31). We previously reported that allelic imbalance of 7q31 is common in prostate cancer and is associated with higher tumor grade and advanced pathologic stage (19).…”

Section: Figurementioning

confidence: 99%

Loss of p53 and c-myc Overrepresentation in Stage T2-3N1-3M0 Prostate Cancer are Potential Markers for Cancer Progression

et al. 2002

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To determine whether genetic changes are markers of cancer progression and patient survival in Stage T 2-3 N 1-3 M 0 prostatic carcinoma, we compared 26 patients who died of tumor relapse after prostatectomy and lymphadenectomy (case group) with 26 matched patients who were alive at the time of the matched case's death (control group). Nine unmatched cases were also included in this study. In 37 cases, paired primary tumors (119 foci) and lymph node metastases (114 foci) were available for study. Fluorescence in situ hybridization (FISH) with centromere-specific probes for chromosomes 7, 8, and 17 and region-specific probes for D7S486 (7q31), c-myc (8q24), LPL (8p22), and p53 (17p13) was performed on available primary carcinomas and lymph node metastases. In primary tumor foci, ؉7q31, ؊8p22, ؉c-myc, substantial additional increases of myc (AI-c-myc), and ؊p53 were observed in 65%, 74%, 43%, 29%, and 31% of foci, respectively. AI-c-myc was strongly associated with higher cancer Gleason score (P ‫؍‬ .003). Heterogeneity of genetic changes was frequently observed among multiple cancer foci. Lymph node metastases of prostate cancer usually shared genetic changes with paired primary tumors. In addition, the genetic change pattern with ؊8p, ؉c-myc or AI-c-myc, ؉7q, and ؉p53 was slightly higher in lymph node metastases (22%) than in primary tumors (6%) (P ‫؍‬ .08). In matched case and control patients, simultaneous gain of 7q31 (؉7q31) and CEP7 (؉CEP7) was identified in 59% and 68% of specimens for case and control groups, respectively (P ‫؍‬ .48). Loss of 8p22 (؊8p22) was identified in 77% and 69% of specimens for case and control groups, respectively (P ‫؍‬ 1.0). Simultaneous gain of c-myc (؉c-myc) and CEP8 (؉CEP8) without overt additional increase of c-myc copy number relative to CEP8 copy number, was identified in 38% and 54% of specimens for case and control groups, respectively (P ‫؍‬ .27). AI-c-myc was identified in 54% and 23% of specimens for case and control groups, respectively (odds ratio ‫؍‬ 3.0, P ‫؍‬ .06). Loss of p53 (؊p53) was identified in 46% and 15% of specimens for case and control groups, respectively (odds ratio Prostate cancer is the most common malignancy and the second leading cause of cancer death in men in the United States (1). Patients with pelvic lymph node metastases of prostatic carcinoma, but no evidence of systemic progression are commonly classified as having Stage T 2-3 N 1-3 M 0 prostate cancer (2). These cancers have an indeterminate natural history (3). Choosing different types of therapy (radiation, surgery, or hormonal therapy) for these

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Section: Figurementioning

confidence: 99%

Loss of p53 and c-myc Overrepresentation in Stage T2-3N1-3M0 Prostate Cancer are Potential Markers for Cancer Progression

et al. 2002

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“…[46][47][48][49] Two other sites on chromosome 10, 10p and 10q26, are also deleted in association with or independent of 10q22-24 losses. 39,[43][44][45] In our study, two loci on 10q, 10q25.1 and 10q25, were examined, but neither showed a significant difference between the relapse and non-relapse groups.…”

Section: Discussionmentioning

confidence: 99%

Allelic imbalance and biochemical outcome after radical prostatectomy

Bott

Masters

Parkinson

et al. 2006

Prostate Cancer Prostatic Dis

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Objective: To compare the incidence of allelic imbalance (AI) in men with rapid disease progression with those who remained disease free after radical prostatectomy, with the aim of identifying genetic markers to predict prognosis and guide further treatment. Patients and methods: Tumour and normal DNA were extracted from two matched groups of 31 men with extracapsular node-negative (pT3N0) prostate cancer who had undergone radical prostatectomy. One group comprised men who developed biochemical recurrence within 2 years of surgery and one group were prostate-specific antigen (PSA) free for at least 3 years. Men were matched for Gleason grade, preoperative PSA and pathological stage. Analysis was performed by genotyping. Results: Allelic imbalance was analysed using 30 markers, and was seen in at least one marker in 57 (92%) of the cases. Deletion at marker D10S211 (10p12.1) was significantly more common in the relapse group than the non-relapse group (35 vs 5%, P ¼ 0.03). Conclusions: This study demonstrates significant association between AI on chromosome 10 and biochemical progression after radical prostatectomy.

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“…The analysis of signal distribution can potentially detect relatively small populations of cells with numerical imbalances in chromosomes. These criteria for both signal distribution and CI were based on published estimates and previous experience of the technique and take into account nuclear truncation Macoska et al, 1993;Baretton et al, 1994;Dinghra et al, 1994;Murphy et al, 1995).…”

Section: Quantitation Of Hybridization Signalsmentioning

confidence: 99%

Increasing genome instability in adrenocortical carcinoma progression with involvement of chromosomes 3, 9 and X at the adenoma stage

et al. 1999

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SummaryThe investigation of chromosomal aberrations in adrenocortical tumours has been limited by the difficulties of applying classical cytogenetics to tumours with low levels of proliferation. We have therefore applied the technique of interphase cytogenetics to paraffin-embedded archival specimens of 14 adrenocortical adenomas and 13 carcinomas. Hybridizations were performed using centromere-specific probes to chromosomes 3, 4, 9, 17, 18 and X, which have been shown to be altered in other types of tumours. Chromosomal imbalance was defined on the basis of changes in both chromosome index (CI) and signal distribution (SD). Where only one of these was altered, this was classified as a tendency to gain or loss. On the basis of the analysis of optimal hybridizations, carcinomas showed gains in all chromosomes studied, five of nine showing gains in multiple chromosomes. Gains were most common in chromosomes 3, 9 and, in particular X, eight of 11 showing gain, and one a tendency to gain. Chromosomal gain was seen less commonly in adenomas, but again chromosomes 3, 9 and X were involved. Losses were infrequent, only one carcinoma showing loss of chromosome 18, and adenomas showing a tendency to loss of chromosomes 4 (two cases), 17 (one case) and 18 (two cases). Our data suggest that changes in chromosomes 3, 9 and X are early events in adrenocortical tumorigenesis, and that there is increasing chromosomal instability with tumour progression.

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Extensive genetic alterations in prostate cancer revealed by dual PCR and FISH analysis

Cited by 68 publications

References 18 publications

Loss of p53 and c-myc Overrepresentation in Stage T2-3N1-3M0 Prostate Cancer are Potential Markers for Cancer Progression

Loss of p53 and c-myc Overrepresentation in Stage T2-3N1-3M0 Prostate Cancer are Potential Markers for Cancer Progression

Allelic imbalance and biochemical outcome after radical prostatectomy

Increasing genome instability in adrenocortical carcinoma progression with involvement of chromosomes 3, 9 and X at the adenoma stage

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